Fatty acid release in incubations of serum with synaptosome and myelin subfractions of brain

1990 ◽  
Vol 68 (1) ◽  
pp. 148-153 ◽  
Author(s):  
R. Roy Baker ◽  
Zou Dao Loh
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Synaptosomal Membranes ◽  
Rat Serum ◽  
Principal Fatty Acid ◽  
Myelin Subfractions ◽  
Fatty Acid Release ◽  
Synaptosomal Plasma Membrane ◽  
Acid Release

To study lipid breakdown in brain membranes following hemorrhage, synaptosome and myelin fractions isolated from rat brain were incubated with rat serum. After 3 h in vitro at 37 °C, 0.43 and 0.26 μmol of fatty acid were released in incubations containing synaptosomes (1.37 μmol phospholipid) or myelin (1.23 μmol phospholipid), respectively, in the presence of 0.25 mL serum. Less than 0.05 μmol of fatty acid was liberated in incubations containing only serum, synaptosomes, or myelin. For synaptosomes and serum, docosahexaenoate was the principal fatty acid released (28 mol% of total) after 3 h of incubation. This fatty acid and arachidonate made up 43 mol% of the liberated fatty acid. The presence of free docosahexaenoate was of interest, as this fatty acid is particularly enriched in phosphatidylserine and phosphatidylethanolamine, phospholipids found in the cytoplasmic half of the synaptosomal plasma membrane and in interior synaptosomal membranes. In incubations of serum and myelin, oleate was the major free fatty acid produced in 30 min to 3 h of incubation (29–35 mol% of total). After 3 h, docosahexaenoate contributed 20 mol% to the total. The release of fatty acids from the membranes may be mediated by serum phospholipase(s) or possibly by activated endogenous lipolytic activities.Key words: fatty acid, serum, synaptosome, myelin, phospholipase A2.

scholarly journals Free fatty acid release from vegetable and bovine milk fat-based infant formulas and human milk during two-phase in vitro digestion

2019 ◽  
Vol 10 (4) ◽  
pp. 2102-2113 ◽  
Author(s):  
Jeske H. J. Hageman ◽  
Jaap Keijer ◽  
Trine Kastrup Dalsgaard ◽  
Lara W. Zeper ◽  
Frédéric Carrière ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Milk Fat ◽  
Bovine Milk ◽  
In Vitro Digestion ◽  
Infant Formulas ◽  
Two Phase ◽  
Fatty Acid Release ◽  
Acid Release

The profile of fatty acids released during in vitro digestion of vegetable and bovine milk fat-based infant formula differ.

Glucose metabolism and mobilization of fatty acids by adipose tissue from obese mice

1961 ◽  
Vol 201 (1) ◽  
pp. 19-22 ◽  
Author(s):  
Bernard Leboeuf ◽  
Serene Lochaya ◽  
Nicole Leboeuf ◽  
Francis C. Wood ◽  
Jean Mayer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Swiss Mice ◽  
Adipose Tissue In Vitro ◽  
Fatty Acid Release ◽  
Acid Release

Free fatty acid mobilization and glucose metabolism to CO2, to glyceride-glycerol, to fatty acids and to glycogen by adipose tissue in vitro were studied in genetically obese hyperglycemic mice (O-H), in goldthioglucose-injected obese Swiss mice and in their respective nonobese littermates. Tissue from O-H mice metabolizes less glucose than tissue from their nonobese littermates in absence of added hormone or in the presence of insulin (0.1 unit/ml) or epinephrine (10–4 m). In addition, there is also a diminished ability for insulin to inhibit and for epinephrine to augment free fatty acid release. No such differences were observed between tissues from goldthioglucose-injected obese Swiss mice and tissues from their lean littermates. Possible significance of these in vitro results with regard to the pathogenesis of the obese hyperglycemic syndrome is discussed.

scholarly journals Biochemical actions of vasoactive peptide hormones. Time-synchronized activation of lipolysis and decreased fatty-acid release by bradykinin and angiotensin in the perfused rabbit kidney

1980 ◽  
Vol 192 (1) ◽  
pp. 127-131 ◽  
Author(s):  
M Schwartzman ◽  
A Raz
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Time Lag ◽  
Rabbit Kidney ◽  
Subsequent Decrease ◽  
Fatty Acid Release ◽  
Initial Activation ◽  
Acid Release ◽  
Sequential Processes ◽  
Vasoactive Peptide

Bradykinin and angiotensin administered to the isolated perfused rabbit kidney activate two sequential processes: (1) a selective release of the prostaglandin precursor arachidonate with concomitant partial conversion of the arachidonate into prostaglandin E2; (2) activation of a process that leads to decreased release of all fatty acids in the perfusate. There is a time lag of approx. 1 min between the initial activation of the arachidonate-specific deacylation reaction that is coupled to prostaglandin generation, and the subsequent decrease in the release of all fatty acids. This synchronized cycle provides for instant generation of required amounts of prostaglandins and at the same time serves to conserve cellular arachidonate.

Epinephrine-insulin antagonism on free fatty acid release

1961 ◽  
Vol 201 (5) ◽  
pp. 815-818 ◽  
Author(s):  
John J. Spitzer ◽  
William T. McElroy
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Blood Sugar ◽  
Drug Administration ◽  
Hepatic Uptake ◽  
Fatty Acid Release ◽  
Plasma Ffa ◽  
Acid Release

The effects of epinephrine or norepinephrine were studied in dogs receiving insulin plus glucose prior to and during administration of the amine. Epinephrine caused a significantly smaller elevation of free fatty acids (FFA) with than without insulin plus glucose administration. Blood sugar responses were quantitatively similar. Epinephrine increased both hepatic uptake of FFA and hepatic release of glucose; these changes were similar to the ones found previously in dogs not receiving insulin plus glucose. The action of norepinephrine on elevating plasma FFA was only slightly and not significantly affected by the administration of insulin plus glucose. When the order of drug administration was reversed, infusion of insulin plus glucose lowered plasma FFA levels and hepatic FFA uptake in animals already receiving either epinephrine or nonepinephrine.

Eicosapentaenoic and dihomo gamma linolenic acid metabolism by cultured rat mesangial cells

1989 ◽  
Vol 256 (1) ◽  
pp. C101-C108 ◽  
Author(s):  
L. A. Scharschmidt ◽  
N. B. Gibbons ◽  
R. Neuwirth
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Acid Metabolism ◽  
Mesangial Cells ◽  
Gamma Linolenic Acid ◽  
Significant Extent ◽  
Glomerular Function ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Stimulation Of

To better understand the effects of dietary fatty acid manipulations on glomerular function, we compared mesangial incorporation, release, and metabolism of arachidonic (AA), eicosapentaenoic (EPA), and dihomo gamma linolenic (DHG) acids. We found marked differences in mesangial handling of these fatty acids. AA was incorporated into lipids of mesangial cells much more rapidly than EPA or DHG. Ionophore-induced stimulation of fatty acid release from mesangial cells prelabeled with [14C]AA, [14C]EPA, or [14C]DHG caused a release of labeled AA greater than DHG much less than EPA, respectively. Preloading mesangial cells with DHG or EPA for 24 h reduced subsequent basal, ionophore-, and hormone-stimulated prostaglandin E2 (PGE2) synthesis. Finally, unlike AA, neither EPA nor DHG was converted to a significant extent by mesangial cyclooxygenase or lipoxygenase. Thus the mesangial metabolism of DHG and EPA differs both quantitatively and qualitatively from that of AA. Furthermore, EPA and DHG inhibit metabolism of AA at the level of mesangial cyclooxygenase.

scholarly journals Vanadium and zinc complexes of 5-cyanopicolinate and pyrazine derivatives: synthesis, structural elucidation and in vitro insulino-mimetic activity study

2017 ◽  
Vol 41 (2) ◽  
pp. 735-746 ◽  
Author(s):  
Tanja Koleša-Dobravc ◽  
Keiichi Maejima ◽  
Yutaka Yoshikawa ◽  
Anton Meden ◽  
Hiroyuki Yasui ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Structural Elucidation ◽  
Zinc Complexes ◽  
Rat Adipocytes ◽  
Fatty Acid Release ◽  
Acid Release

Inhibition of free fatty acid release from rat adipocytes was observed for vanadium(iv), vanadium(v) and zinc(ii) complexes.

Effect of calcium on the kinetics of free fatty acid release during in vitro lipid digestion in model emulsions

2013 ◽  
Vol 139 (1-4) ◽  
pp. 681-688 ◽  
Author(s):  
Aiqian Ye ◽  
Jian Cui ◽  
Xiangqian Zhu ◽  
Harjinder Singh
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Lipid Digestion ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Kinetics Of

Action of phospholipases A2 and C on free fatty acid release during complete ischemia in rat neocortex

1992 ◽  
Vol 76 (4) ◽  
pp. 648-651 ◽  
Author(s):  
Atsushi Umemura ◽  
Hideo Mabe ◽  
Hajime Nagai ◽  
Fumihiko sugino
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Phospholipase C ◽  
Phenylmethylsulfonyl Fluoride ◽  
Content Type ◽  
Rat Neocortex ◽  
Fatty Acid Release ◽  
Acid Release

✓ The levels of brain free fatty acids rapidly increase after the onset of ischemia. The purpose of this study was to investigate the action of phospholipases A2 and C during complete ischemia based on the effects of a phospholipase C inhibitor (phenylmethylsulfonyl fluoride) and the N-methyl-D-aspartate antagonist MK-801 on the release of free fatty acids in rat neocortex. Complete brain ischemia was induced in rats with cardiac arrest by intracardiac injection of KC1. Free fatty acid levels in the neocortex were measured 0, 2, 4, and 8 minutes after cardiac arrest. Phenylmethylsulfonyl fluoride inhibited the release of free fatty acids primarily from phosphatidylinositol during the first 2 minutes of ischemia and from phosphatidylcholine and phosphatidylethanolamine at 4 to 8 minutes of ischemia. Conversely, MK-801 inhibited free fatty acid release mainly from phosphatidylcholine and phosphatidylethanolamine at 2 to 4 minutes of ischemia. These results indicate that the release of free fatty acids during the first 2 minutes of ischemia can be attributed mostly to the action of phospholipase C, and that the activation of phospholipase C further influences the activation of phospholipase A2 in the subsequent course, while phospholipase A2 predominantly acts after 2 minutes of ischemia.

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